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Next Generation Sequencing Facilitates Quantitative Analysis of MYC+ and MYC+ SETD2-/- Renal Tubular Cells Transcriptomes

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of MYC+ and MYC+ SETD2-/- Renal Tubular Cells Transcriptomes

PROVIDER: PRJNA516015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8464900_1.fastq.gz	Fastqsanger.gz
	SRR8464900_2.fastq.gz	Fastqsanger.gz
	SRR8464901_1.fastq.gz	Fastqsanger.gz
	SRR8464901_2.fastq.gz	Fastqsanger.gz
	SRR8464898_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of MYC+ and MYC+; SETD2-/- Renal Tubular Cells Transcriptomes

Project description:To get an insight into the mechanism of how SETD2 ablation promotes ccRCC, we performed RNA-seq using the renal tubules isolated from MYC+; SETD2-/- mice compared with their control MYC+ littermates.

2020-12-31 | GSE125381 | GEO

RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in mice.

Project description:To explore a possible role of SETD2 in kidney development and tumorigenesis in vivo, we generated Setd2-floxed mice and deleted the Setd2 gene in tubular epithelial cells using a transgenic Ksp1.3/Cre mouse line. Then, we established our own c-MYC-transgene mouse line by overexpressing the human c-MYC under the control of the Ksp promoter to generate kidney disease mouse model. To get an insight into the mechanism of how SETD2 ablation promotes ccRCC formation in a c-MYC-generated PKD model, we performed RNA-seq using the renal tubules isolated from Wild Type, Setd2-KO, MYC-OE and MYC-OE; Setd2-KO mice.

2021-03-14 | GSE168849 | GEO

RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines

Project description:RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines. Examination of RNA expression in SETD2 isogenic cell lines

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Gene expression analysis of murine renal tubular epithelial cells upon SETD2 knockout [RNAseq_RTE]

Project description:SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24 of 51 (47%) metastatic ccRCC tumors. Using SETD2-mutant metastatic ccRCC patient-derived cell line and xenograft models, we showed that H3K36me3 restoration greatly reduced distant metastases of ccRCC in mice. An integrated ATAC-seq, ChIP-seq, and transcriptome analysis concluded a tumor suppressor model in which loss of SETD2-mediated H3K36me3 activates enhancers to drive oncogenic transcription through dysregulating histone chaperone recruitment, enhancing histone exchange, and expanding chromatin accessibility. Furthermore, we uncovered mechanism-based therapeutic strategies for SETD2-deficient cancer through inhibition of histone chaperones. Overall, SETD2-loss creates a permissive epigenetic landscape for cooperating oncogenic drivers to amplify transcriptional output, providing unique therapeutic opportunities.

2021-11-15 | GSE146541 | GEO

Chromatin landscape analysis of murine renal tubular epithelial cells upon SETD2 knockout [ATACseq_RTE]

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Gene expression analysis of murine renal tubular epithelial cells upon SETD2 knockout [RNAseq_RTE]

Project description:Gene expression analysis of murine renal tubular epithelial cells upon SETD2 knockout [RNAseq_RTE]

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Chromatin landscape analysis of murine renal tubular epithelial cells upon SETD2 knockout [ATACseq_RTE]

Project description:Chromatin landscape analysis of murine renal tubular epithelial cells upon SETD2 knockout [ATACseq_RTE]

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Cloning and variation of adult renal tubular progenitors

Project description:Kidney damage involves the progressive and inexorable destruction of tubular and glomerular system. However, it is known that the patients survive AKI often recover renal structure and function. Correspondingly, previous studies demonstrated tubular regeneration in mice after massive kidney injury and linked mouse Sox9+ renal progenitor cells to this process. Here we show that renal progenitor cells can be cloned from renal needle biopsy sample of CKD patients. Progenitor cells can readily assembly into “kidney organoids” expressing proximal/distal tubular cell markers in 3D culture.

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Project description:RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines.

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Dynamic Reprogramming of DNA Methylation in SETD2-Deregulated Renal Cell Carcinoma

Project description:Clear cell renal cell carcinomas (ccRCCs) harbor frequent mutations in epigenetic modifiers including SETD2, the writer for H3K36me3. We profiles DNA methylation across cell line models of SETD2 inactivation and SETD2 mutated primary tumors as this epigenetic mark is linked to H3K36me3 and is a targetable mark for cancer therapy. SETD2 depleted cell line models (long-term and acute) exhibited a hypermethylation phenotype coinciding with ectopic gains in H3K36me3 centered across intergenic regions adjacent to low expression genes that became upregulated with dysregulation of the epigenome. Poised enhancers of developmental genes demonstrated enrichment for the hypermethylation phenotype. Deregulation of the epigenome observed in the cell line models was recapitulated in SETD2 mutated primary ccRCC, papillary renal cell carcinomas, and lung adenocarcinomas.

2015-09-30 | GSE70645 | GEO

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